When functioning property, the human heart maintains its own intrinsic rhythm and will pump an adequate supply of blood throughout the body's circulatory system. However, some individuals have cardiac arrhythmias and/or disease states that result in diminished blood circulation. One method of treating cardiac arrhythmias is the administration of drug therapy. Another method is the use of a cardiac rhythm management system. Such systems (pacemakers, cardioverters, among others) are usually implanted in the patient and deliver electrical stimulation therapy directly to the heart.
One type of cardiac disturbance faced by cardiac rhythm management systems is congestive heart failure (CHF). CHF is a condition in which the muscles in the walls of the right and/or left sides of the heart are stretched abnormally with each cardiac filling and contraction. As a result, the left atrium and left ventricle become enlarged, and the heart muscle possesses less contractility, a condition called left ventricular dysfunction (LVD). LVD decreases cardiac output, which, in turn, often results in an increased heart rate with less resting time between contractions. The heart consumes more oxygen, and its condition, along with the patient's, typically worsens over a period of time.
When the left side of the heart has become enlarged due to CHF, the ventricular depolarization signals may travel through and depolarize the left side of the heart more slowly than they do in the right ventricle. As a result, the left and right ventricles do not contract simultaneously. Rather, the left ventricle contracts somewhat later than the right ventricle. This further reduces the pumping efficiency of the heart.
As a result, there has been a need to provide CHF patients with a pacing therapy that coordinates ventricular contractions or otherwise increases the heart's pumping efficiency. Moist recently, atrial synchronous pacing that provides simultaneous pacing pulses to both right and left ventricles has met this need.
In general, LVD with conduction disturbances patients benefit from pacing pulses applied simultaneously in both right and left heart chambers. These ventricular pacing pulses must be delivered in synchrony with atrial paced or sensed depolarizations detected at the atrial electrode site(s). The programmed AV interval durations following atrial paced or sensed events must also be short enough to rule out spontaneous, conducted R-waves. Atrial and left ventricular cardiac output can be significantly improved when left and right chamber synchrony is restored, particularly in patients suffering from dilated cardiomyopathy, LVD, and CHF.
A number of proposals have been advanced for providing pacing therapies to alleviate heart failure conditions and restore synchronous depolarization and contraction of a single heart chamber, right and left, or upper and lower heart chambers as described in detail in the commonly assigned U.S. Pat. No. 6,129,744 and in commonly assigned U.S. Pat. Nos. 5,403,356, 5,797,970, 5,902,324, and 6,070,100 and U.S. Pat. Nos. 5,720,768 and 5,792,203. The proposals appearing in U.S. Pat. Nos. 3,937,226, 4,088,140, 4,548,203, 4,458,677, 4,332,259 are summarized in U.S. Pat. Nos. 4,928,688 and 5,674,259. The advantages of providing sensing at pace/sense electrodes located in both the right and left heart chambers is addressed in the '688 and '259 patents, as well as in U.S. Pat. Nos. 4,354,497, 5,174,289, 5,267,560, 5,514,161, and 5,584,867. Maintenance of AV mechanical synchrony is of great importance as set forth in greater detail in commonly assigned U.S. Pat. No. 5,626,623, incorporated herein by reference in its entirety.
Other intervals timed by the implantable pulse generator (IPG) include atrial and ventricular sense amplifier blanking periods following delivery of atrial and/or ventricular pacing pulses to disable atrial and ventricular sensing. In addition, sense amplifier refractory periods are timed out following atrial and ventricular paced and sensed event signals. Such “refractory” A-SENSE and V-SENSE signals are selectively ignored or employed in a variety of ways to reset or extend time periods. An atrial refractory period (ARP) extends for various time durations through the Sensed AV (SAV) delay or the Paced AV (PAV) delay.
In addition, a post-ventricular atrial refractory period (PVARP) begins at a V-PACE pulse or V-SENSE. A-SENSE signals sensed during the PVARP are noted but do not start an AV interval. The rationale for this operation is that such events may be a retrograde atrial sensed event or an event that is part of an atrial tachycardia episode. In either case, it is not desirable to synchronize ventricular pacing to such events. The duration of the PVARP may be fixed by programming, extended after a premature ventricular contraction (PVC), or vary as a function of the pacing or heart rate, with the result that in many cases relatively long PVARPs are in effect at lower rates.
The atrial tracking VDD/R and DDD/R pacing modes function in the above-described manner and additionally provide rate modulation of a ventricular pacing escape interval between a programmable lower rate and an upper rate limit (URL). The URL may either be the upper tracking rate (UTR) or upper sensor rate (USR). At times when the intrinsic atrial rate is increasing due to exertion, the SAV is extended to prevent the ventricular pacing rate from exceeding the UTR through an operation commonly termed “Pacemaker Wenckebach.” The atrial rate, however, may continue to rise until native atrial events fall into the PVARP. At such times, if the patient has a conduction block, the ventricular paced beat is “blocked” since the refractory sensed atrial event cannot start an SAV interval. If, however, the patient has an intact AV conduction system, a native ventricular depolarization may occur. This operation is described in U.S. Pat. No. 6,256,536 which is incorporated herein by reference in its totality.
The disruption of AV electrical and mechanical synchrony frequently arises due to the spontaneous depolarization of the ventricles triggered at an ectopic site in one of the ventricles. Such a spontaneous depolarization that is not associated with a prior atrial depolarization is characterized as a PVC. Many of the problems resulting from the occurrence of a PVC in a patient with a dual chamber pacemaker are described more fully in U.S. Pat. Nos. 4,788,980 and 5,097,832, both of which are incorporated herein by reference. One such problem is the initiation of a pacemaker mediated tachycardia or PMT. The most commonly employed PVC response to prevent initiation of PMT is to extend the PVARP to a programmed duration, such as 400-500 ms, in response to the PVC. Moreover, a “pacemaker-defined” PVC is defined as the second of two ventricular events without an intervening atrial event. Such a pacemaker-defined PVC also extends an associated PVARP to 400, 500, or more milliseconds (ms). The PVARP extension masks atrial sensed signals that are presumed to result from retrograde conduction during this period of time as disclosed in the above-incorporated '980 patent. Numerous other patents have dealt with varying the PVARP in an attempt to prevent instigating a PMT, including U.S. Pat. Nos. 6,167,307, 5,653,738, 4,920,965, 4,554,921, 5,123,412, and 4,503,857, all incorporated herein by reference in their entireties.
Unfortunately, in some circumstances prolongation of the PVARP in response to a PVC or prolongation of the SAV interval (Wenckebach operation) has unfortunate consequences. Even though a possible PMT is prevented, loss of normal P-wave tracking [atrial sense-ventricular pace (AS-VP)] may occur because the P-wave occurs during the PVARP.
If the subsequent PVARP is long enough, a P-wave may fail to initiate an SAV delay. If, however, normal AV conduction is present, a native ventricular depolarization will occur [atrial refractory (AR-VS)]. Such native ventricular depolarization, however, interrupts CHF therapy that requires ventricular pacing. Loss of this type of atrial synchrony may extend over a period of time (e.g., seconds to hours) depending on the pacemaker's programmed rate settings and the patient's sinus rate (i.e., the P-wave rate set by the SA node). Ventricular pacing remains inhibited until either the occurrence of an non-refractory sensed atrial depolarization or delivery of an atrial pacing pulse outside the total atrial refractory period (TARP).
A similar problem may arise in response to other events that disrupt AV synchrony. Additional events which disrupt AV synchrony include, among others, premature atrial contractions, noise sensing and associated asynchronous pacing, also known as “noise reversion” and other pacing mode or operation changes, including those arising from mode switching, telemetric programming (e.g., placing a magnetic field proximate a pacemaker), removal of a magnetic field, “cancel magnet” commands, device programming and downlink telemetry functions. In particular, changes from non-atrial synchronized pacing modes to atrial synchronized pacing modes or from non-atrial synchronized operation to atrial synchronized operation within an atrial synchronized pacing mode have the potential to disrupt AV synchrony. Prolongation of PVARP in response to such disrupting events is disclosed in U.S. Pat. No. 4,554,920, also incorporated herein by reference in its entirety.
In modern dual chamber pacemakers, the programmed initial PVARP may vary as a function of the heart rate or sensor rate. In the context of these types of pacemakers, the relatively long PVARPs that may be in effect at lower rates can, in the same fashion, result in persistent loss of AV synchrony as described above. A method, that resolves these issues for most implantable medical devices (IMDs), but not CHF devices, has been disclosed in U.S. Pat. No. 6,311,088, incorporated herein by reference in its entirety.
U.S. Pat. No. 5,741,309 provides one solution to correcting this problem in CHF IMDs. This patent employs the term PR+PVARP block to define the conduction of an AR event to the ventricles resulting in a ventricular sense. The solution is stated as follows: “After a predetermined number of cycles where an atrial event is sensed during a PVARP, the pacemaker is programmed to ignore or shorten the PVARP and/or URI, pacing the ventricles after the next sensed AV event thereby breaking the PR+PVARP block.” While shortening the PVARP or upper rate interval may be applicable, the inventors of the present invention believe that ignoring or shortening either or both may lead to other pacing problems during the time that either or both are ignored or shortened. Otherwise, this patent disclosure offers little detail on how or when the programmed PVARP or URI is restored.
Holter recordings have revealed extended periods of time during which cardiac resynchronization therapy (CRT) is not continuously delivered. For the purposes of the present disclosure CRT can be considered a form of triple chamber, synchronized bi-ventricular pacing. The cardiac rhythm that was observed to cause this lack of continuous CRT delivery was atrial refractory sense to ventricular sense (AR-VS). That is, whenever an atrial event falls within the refractory portion of the PVARP it cannot start an AV interval and, thus, cannot be tracked. There are several causes that may start such a rhythm and may be listed, among others, as follows.
The patient's atrial rate exceeds the programmed upper tracking rate (UTR). As a result, atrial events fall within the PVARP. As a result and assuming the presence of intrinsic AV conduction, the atrial depolarization is conducted to the ventricle(s), resulting in an intrinsic ventricular depolarization. Since the intrinsic AV conduction is longer than the programmed SAV, the overall TARP (AV conduction and PVARP) causes the next atrial event to occur during the PVARP, and, though sensed during the PVARP, no SAV interval is initiated. Once this cardiac rhythm pattern (AR-VS) is established, the atrial rate must decrease to the point that the atrial event no longer falls into the PVARP in order for the AR-VS pattern to terminate. That is, as soon as an atrial event is sensed outside of refractory, a SAV is initiated and tracking restored. For example, with intrinsic AV conduction of 300 ms and a PVARP programmed to 310 ms, the atrial rate must fall below 100 bpm before atrial tracking is restored, thereby resuming CRT delivery.
Multiple PVCs or PVC couplets may also cause an AR-VS pattern. Although the first PVC may trigger a long PVARP, e.g., 400 to 500 ms, the P-wave that falls into the refractory period may be conduced to the ventricles, leading to an AR-VS pattern.
Similarly, an undersensed atrial event that conducts, resulting in an R-wave that is a “pacemaker-defined” PVC, may cause the next atrial event to occur during a PVARP and bring about a second conducted R-wave. The AR-VS pattern may continue if the patient's atrial rate is fast enough.
An atrial tachyarrhythmia may often result in an AR-VS pattern with a rate faster than the UTR. If the tachyarrhythmia breaks with the atrial rate slowing below the UTR, the first atrial depolarization may occur during a refractory period and start the AR-VS pattern.
What is needed, then, is a method for identifying the AR-VS pattern and restoring atrial tracking as quickly as possible. Thus, the basis for the loss of cardiac resynchronization therapy is resolved.